Repetitive static muscle contractions in humans ?a trigger of metabolic and oxidative stress?

Abstract
Repetitive static exercise (RSE) is a repetitive condition of partial ischaemia/reperfusion and may therefore be connected to the formation of oxygen-derived free radicals and tissue damage. Seven subjects performed two-legged intermittent knee extension exercise repeating at 10 s on and 10 s off at a target force corresponding to about 30% of the maximal voluntary contraction force. The RSE was continued for 80 min (n=4) or to fatigue (n=3). Four of the subjects also performed submaximal dynamic exercise (DE) at. an intensity of about 60% maximal oxygen uptake (VO2max) for the same period. Whole body oxygen uptake (VO2) increased gradually with time during RSE (PPVO2 during submaximal cycling. Maximal force (measured in six additional subjects) declined gradually during RSE and was not completely restored after 60 min of recovery. After 20 and 80 min (or at fatigue) RSE phosphocreatine (PC) dropped to 74% and 60% of the initial value, respectively. A similar decrease in PC occurred during DE. Muscle and arterial lactate concentrations remained low during both RSE and DE. The three subjects who were unable to continue RSE for 80 min showed no signs of a more severe energy imbalance than the other subjects. A continuous release of K+ occurred during both RSE and DE. The total muscle loss of K+ was about 3% and 6% of the total muscle K+ content during RSE and DE, respectively. Muscle glutathione, glutathione disulphide, ubiquinone and α-tocopherol are involved in the cellular defence system against free radicals. During RSE and DE these parameters were unchanged and plasma malondialdehyde (a product of free radical induced lipid peroxidation) remained below the detection limit. In conclusion, prolonged RSE resulted in a gradual decrease in PC, mechanical efficiency and maximal force. There were no signs of an enhanced rate of free radical formation.